ライフサイエンスコーパス: 1-methyl-4-phenylpyridinium

1 of "prototypical" Oct substrates, including 1-methyl-4-phenylpyridinium.

2 ibition of reactive microgliosis elicited by 1-methyl-4-phenylpyridinium.

3 ibition of reactive microgliosis elicited by 1-methyl-4-phenylpyridinium.

4 and cimetidine while retaining transport of 1-methyl-4-phenylpyridinium.

5 T), including 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium.

6 the specific uptake of the organic cation 3H-1-methyl-4-phenylpyridinium (3H-MPP+) was significantly

7 ese studies we use a fluorescent analogue of 1-methyl-4-phenylpyridinium, a neurotoxic metabolite and

8 hat mOat3 transports organic cations such as 1-methyl-4-phenylpyridinium and cimetidine.

9 eriments were conducted using [(3)H] MMP(+) (1-methyl-4-phenylpyridinium) as the marker ligand and va

10 of organic cations, including the neurotoxin 1-methyl-4-phenylpyridinium, as substrates.

11 T, but not TAT-C24Scr, decreased AMPH-evoked 1-methyl-4-phenylpyridinium efflux.

12 pers the release of the toxic organic cation 1-methyl-4-phenylpyridinium from astrocytes and protects

13 produced significant neuroprotection against 1-methyl-4-phenylpyridinium, glutamate, and nitric oxide

14 ol DA neurons were comparably susceptible to 1-methyl-4-phenylpyridinium-, glutamate-, or camptotheci

15 of the fixed cations, tetraethylammonium and 1-methyl-4-phenylpyridinium, i.e. the pH value did not h

16 lyinosinic-polycytidylic acid)-, HIV-1 Tat-, 1-methyl-4-phenylpyridinium(+)-, IL-1beta-, and IL-12 p4

17 verexpression confers protection by blocking 1-methyl-4-phenylpyridinium-induced CHOP up-regulation,

18 n, renders PC12 and MN9D cells vulnerable to 1-methyl-4-phenylpyridinium-induced cytotoxic cell death

19 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/1-methyl-4-phenylpyridinium-induced dopaminergic neuroto

20 eptor agonist, significantly reduced LPS- or 1-methyl-4-phenylpyridinium-induced dopaminergic neuroto

21 iated mitophagy and protects neurons against 1-methyl-4-phenylpyridinium-induced oxidative stress in

22 nhibited H(2)O(2) and the Parkinsonian toxin 1-methyl-4-phenylpyridinium-induced PKCdelta cleavage, k

23 mine oxidase type B)-catalyzed production of 1-methyl-4-phenylpyridinium ion (MPP(+)) and is likely t

24 cells treated with an exogenous neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP(+)) significantly d

25 catalyzes the oxidation of MPTP to the toxic 1-methyl-4-phenylpyridinium ion (MPP(+)), which then tar

26 s in striatal pharmacokinetics or content of 1-methyl-4-phenylpyridinium ion (MPP+), the active metab

27 in axons challenged with the DA neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP+).

28 to complex I inhibitors such as rotenone and 1-methyl-4-phenylpyridinium ion, known as a metabolite o

29 ded complex I inhibitor such as rotenone and 1-methyl-4-phenylpyridinium ion.

30 opamine (K(m) = 329 mum), and the neurotoxin 1-methyl-4-phenylpyridinium (K(m) = 33 mum).

31 1-Methyl-4-phenylpyridinium, lipopolysaccharide (LPS), a

32 tudy, using the well-established LPS and the 1-methyl-4-phenylpyridinium-mediated models of Parkinson

33 dative stress, and neurotoxicity produced by 1-methyl-4-phenylpyridinium (MPP(+)) and 6-hydroxydopami

34 r modeling to compare fluorescent analogs of 1-methyl-4-phenylpyridinium (MPP(+)) as reporters for th

35 cells treated with the parkinsonian toxicant 1-methyl-4-phenylpyridinium (MPP(+)) as well as in the s

36 ttenuates amphetamine-triggered DAT-mediated 1-methyl-4-phenylpyridinium (MPP(+)) efflux.

37 ease of mitochondrial calcium in response to 1-methyl-4-phenylpyridinium (MPP(+)) in human neuroblast

38 rgic stress and by dopaminergic neurotoxins, 1-methyl-4-phenylpyridinium (MPP(+)) in vitro and in viv

39 1-Methyl-4-phenylpyridinium (MPP(+)) is a neurotoxin tha

40 1-Methyl-4-phenylpyridinium (MPP(+)) is selectively toxi

41 The neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) produces mitochondr

42 vitro by challenging dopaminergic cells with 1-methyl-4-phenylpyridinium (MPP(+)), a neurotoxin that

43 ated the molecular mechanisms of toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), an ultimate toxic

44 Uptake of the Parkinsonism-inducing toxin, 1-methyl-4-phenylpyridinium (MPP(+)), into dopaminergic

45 porter (VMAT), and a charged VMAT, substrate 1-methyl-4-phenylpyridinium (MPP(+)), reduced striatal C

46 e localization and transport activity toward 1-methyl-4-phenylpyridinium (MPP(+)), serotonin (5-HT),

47 1-Methyl-4-phenylpyridinium (MPP(+)), the active metabol

48 1-Methyl-4-phenylpyridinium (MPP(+)), the toxic metaboli

49 easuring accumulation of radiolabeled DA and 1-methyl-4-phenylpyridinium (MPP(+)), was found to direc

50 Using models of serum deprivation and 1-methyl-4-phenylpyridinium (MPP(+)), we investigated th

51 eath of neurons treated with the neurotoxin, 1-methyl-4-phenylpyridinium (MPP(+)), which induces conv

52 display similar relative effects in blocking 1-methyl-4-phenylpyridinium (MPP(+))-mediated death of d

53 a demonstrate that minocycline inhibits both 1-methyl-4-phenylpyridinium (MPP(+))-mediated iNOS expre

54 gic cell lines using the mitochondrial toxin 1-methyl-4-phenylpyridinium (MPP(+)).

55 The compound 1-methyl-4-phenylpyridinium (MPP) is a selective inhibit

56 ; and two prototypic cationic substrates, 3) 1-methyl-4-phenylpyridinium (MPP), and 4) the novel fluo

57 Using 1-methyl-4-phenylpyridinium (MPP+) -treated C57 mice pri

58 ute (48 h) exposure to the neurotoxic agents 1-methyl-4-phenylpyridinium (MPP+) and N-methyl-D-aspart

59 , OCT3 mediates the uptake of the neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and the neurotransmit

60 g neurotoxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP+) in a dopaminergic cel

61 ,2,3,6-tetrahydropyridine and its metabolite 1-methyl-4-phenylpyridinium (MPP+) induce PD symptoms an

62 t growth factor (bFGF) could protect against 1-methyl-4-phenylpyridinium (MPP+) induced striatal dama

63 1-Methyl-4-phenylpyridinium (MPP+) levels after MPTP adm

64 vity, and (3) significantly greater striatal 1-methyl-4-phenylpyridinium (MPP+) levels, as compared t

65 IRIP overexpression inhibited endogenous 1-methyl-4-phenylpyridinium (MPP+) uptake activity in He

66 ere treated with the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP+), and GM1 ganglioside

67 -4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridinium (MPP+), exerts its lethal ef

68 ture similar to the dopaminergic neurotoxin, 1-methyl-4-phenylpyridinium (MPP+), has been shown to pr

69 entral midbrain neurons treated with 6-OHDA, 1-methyl-4-phenylpyridinium (MPP+), or alpha-synuclein f

70 gically induced Parkinson's disease involves 1-methyl-4-phenylpyridinium (MPP+), the active metabolit

71 g its effects by altering striatal levels of 1-methyl-4-phenylpyridinium (MPP+), the active metabolit

72 1-Methyl-4-phenylpyridinium (MPP+), the cytotoxic metabo

73 herbicide with chemical structure similar to 1-methyl-4-phenylpyridinium (MPP+), the MPTP metabolite

74 de (PrP)-, dsRNA (poly IC)-, HIV-1 Tat-, and 1-methyl-4-phenylpyridinium (MPP+)-, but not IFN-gamma-,

75 uronal toxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridinium (MPP+).

76 noamine neurotransmitters and the neurotoxin 1-methyl-4-phenylpyridinium (MPP+).

77 aminergic neurons to the complex I inhibitor 1-methyl-4-phenylpyridinium (MPP+).

78 -11 of hENT1 behaved like PMAT, transporting 1-methyl-4-phenylpyridinium (MPP+, an organic cation) bu

79 sensitization to dopaminergic loss following 1-methyl-4-phenylpyridinium/MPTP treatment, in vitro and

80 Upon injury with the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium, N27 cells (dopaminergic neu

81 chondrial complex I inhibitors (rotenone and 1-methyl-4-phenylpyridinium or MPP(+)) on striatal and c

82 The neurotoxin MPP+ (1-methyl-4-phenylpyridinium), oxidative stress, or impai

83 derivatives with tyramine and the neurotoxin 1-methyl-4-phenylpyridinium suggest that the flexibility

84 desipramine, and quinidine, but not by MPP+ (1-methyl-4-phenylpyridinium), TEA (tetraethylammonium),

85 activates Bim, and induces apoptosis only in 1-methyl-4-phenylpyridinium-treated cells.

86 This binding is lost following 1-methyl-4-phenylpyridinium treatment.

87 the uptake of monoamines and the neurotoxin 1-methyl-4-phenylpyridinium was significantly reduced in

88 A neurons exposed to the mitochondrial toxin 1-methyl-4-phenylpyridinium were also partially protecte

89 res from Parkinson's disease-relevant toxin, 1-methyl-4-phenylpyridinium, whereas downregulation of o